Acute M1 Myeloid Leukemia (Acute Myeloblastic Leukemia without Maturation)

Acute M1 myeloid leukemia is a fast-growing blood cancer that starts in very early myeloid cells (myeloblasts) inside the bone marrow. In this subtype, the blasts dominate the marrow and show little to no maturation into neutrophils. By classic FAB (French-American-British) criteria, marrow cells are mostly blasts, fewer than 10% of cells show granulocytic maturation, and at least 3% of blasts stain positive for myeloperoxidase (MPO) or Sudan Black B, proving a myeloid origin; if MPO/SBB is <3% it belongs to a different subtype (M0, “minimal differentiation”). Today, modern systems (WHO-2022/ICC-2022) emphasize genetic and immunophenotypic features rather than FAB labels, but this morphologic picture still helps describe disease biology. MedscapeNCBIPMCCollege of American Pathologists

Acute myeloid leukemia (AML) M1 is a fast-growing blood cancer in which very early myeloid cells (called blasts) build up in bone marrow and blood. In M1, blasts do not mature into working neutrophils; maturing granulocytes make up <10% of marrow cells. Because the marrow is packed with blasts, normal blood cell production falls, causing anemia, infections, and bleeding. Diagnosis relies on bone marrow biopsy, immunophenotyping/flow cytometry, and genetic testing to guide therapy and prognosis. While FAB M1 is a morphology label, modern care is driven by molecular findings (FLT3, NPM1, IDH1/2, KMT2A, etc.) and fitness for intensive therapy. SEERNational Organization for Rare DisordersMedscape

Acute M1 myeloid leukemia is a fast leukemia of the myeloid line where immature cells multiply quickly but cannot grow up into normal white cells. The bone marrow becomes crowded, so red cells drop (tiredness, shortness of breath), platelets drop (easy bruising, bleeding), and neutrophils drop (fever and infections). Doctors confirm the disease with blood tests, marrow tests, and flow cytometry that shows myeloid markers. They also run chromosome and mutation tests to pick the right treatment plan. Modern treatment may use chemotherapy, targeted pills, antibody-drug conjugates, and stem cell transplant, plus strong supportive care to prevent infection and bleeding. The goal is to reach complete remission, then keep it away with more chemo, targeted drugs, or allogeneic transplant depending on risk. ASH PublicationsNCCN

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Other names

This disease has been called Acute myeloblastic leukemia without maturation, Acute myeloid leukemia M1, FAB M1, and simply AML without maturation. These names come from the older FAB system that grouped AML by how “mature” the leukemia cells look under the microscope and what stains they pick up (like MPO/Sudan Black B). In newer classifications (WHO-2022, ICC-2022), the exact FAB name is used less, and the case is categorized mainly by its gene changes and immunophenotype, but clinicians still use “M1” informally to communicate this “many blasts, little maturation” pattern. SEERCollege of American Pathologists

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Types

1. De novo vs secondary (therapy-related or MDS-related).
   De novo appears without a known prior marrow disease. Secondary follows chemotherapy/radiation or evolves from a myelodysplastic/myeloproliferative disorder. This split matters because secondary/therapy-related cases often carry adverse-risk genetics and behave more aggressively. Cancer.gov

2. Genetically defined risk groups (ELN-2022).
   At diagnosis, AML is risk-stratified by key mutations and fusions (e.g., NPM1, FLT3-ITD, ASXL1, RUNX1, TP53, complex karyotype). These determine “favorable,” “intermediate,” or “adverse” risk and guide treatment, regardless of the FAB look. ASH PublicationsPMCNature

3. WHO-2022 / ICC-2022 mapping.
   FAB M1 no longer sits as a standalone entity. The same case is classified under WHO-2022/ICC-2022 using genetic drivers and blast percentage (usually ≥20%), with categories like “AML with recurrent genetic abnormalities” or “AML, defined by differentiation, NOS.” The M1 morphology still describes “without maturation.” College of American PathologistsPMCBioMed Central

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Causes/risk factors

Strict “single causes” are rare; most are risk factors that raise the chance of getting AML with an M1 pattern.

1. Older age. Risk of AML rises with age due to lifelong DNA damage in marrow stem cells. Cancer.gov

2. Previous chemotherapy (alkylating agents, topoisomerase II inhibitors). Prior cancer treatment can injure marrow DNA and lead to therapy-related AML, often high-risk. Cancer.gov

3. Radiation exposure. High-dose ionizing radiation (past radiotherapy or major environmental exposure) increases AML risk years later. Wikipedia

4. Benzene and similar solvents. Long-term exposure can damage marrow cells and raise AML risk. Cancer.gov

5. Smoking. Tobacco smoke contains benzene and other carcinogens that raise AML risk. Cancer.gov

6. Prior myelodysplastic syndrome (MDS). MDS can evolve (“transform”) into AML; such cases are often genetically adverse. Cancer.gov

7. Myeloproliferative neoplasms (e.g., polycythemia vera). These can also transform into AML. Cancer.gov

8. Down syndrome and other inherited syndromes (Fanconi anemia, Bloom, ataxia-telangiectasia, severe congenital neutropenia). They carry higher leukemia risk due to DNA-repair problems. Wikipedia

9. Family platelet disorder with RUNX1 mutation. This rare inherited condition predisposes to AML. Cancer.gov

10. GATA2 deficiency. A germline defect in a key hematopoietic gene predisposes to MDS/AML. Cancer.gov

11. Li-Fraumeni syndrome (TP53). Germline TP53 changes impair DNA repair and increase AML risk. Cancer.gov

12. Aplastic anemia (especially post-therapy). Damaged marrow and prior immunosuppressive treatment can precede AML. Cancer.gov

13. Obesity. Chronic inflammation and altered cytokines may slightly increase AML risk. Wikipedia

14. Certain occupations (historically: nuclear industry, electronics manufacturing, animal processing) with chemical/radiation exposures. Wikipedia

15. Male sex (small effect). Some series show a modest male predominance in AML overall. Cancer.gov

16. Prior radiation accidents/atomic exposures (historic cohorts). Long-term studies showed higher AML rates. Wikipedia

17. Chronic immune dysregulation. Longstanding immune activation and marrow stress may contribute to clonal evolution. (Inference consistent with MDS/autoimmune links.) Cancer.gov

18. Environmental pesticides/solvents (mixed evidence). Some epidemiology suggests higher AML risk. Cancer.gov

19. Clonal hematopoiesis of indeterminate potential (CHIP). Age-related mutations can be a stepping stone to AML in some people. (Modern frameworks discuss this risk.) ASH Publications

20. Unknown/idiopathic. Many patients have no clear exposure or syndrome; spontaneous mutations accumulate and trigger AML. Cancer.gov

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Common symptoms & signs

1. Tiredness and weakness. Too few red blood cells (anemia) carry less oxygen, causing fatigue and low energy. Cancer.gov

2. Pale skin. Anemia reduces hemoglobin, so skin looks paler than usual. Cancer.gov

3. Shortness of breath on exertion. Low oxygen delivery makes even light activity feel breathless. Rogel Cancer Center

4. Fever. Infection is common because healthy white cells are low; fever can also arise from leukemia-related inflammation. Cancer.gov

5. Frequent or severe infections. Neutropenia and dysfunctional leukocytes reduce immune defense. Cancer.gov

6. Easy bruising and bleeding (nosebleeds, gum bleeding). Platelets are low or not working well, so bleeding starts easily and stops slowly. Cancer.gov

7. Petechiae (tiny red spots). These pinpoint skin spots are small bleeds from low platelets. Rogel Cancer Center

8. Bone or joint pain. Marrow packed with blasts raises pressure and irritates nerves. Cancer.gov

9. Weight loss and low appetite. Active cancer increases energy use and reduces appetite. Rogel Cancer Center

10. Night sweats. Systemic inflammation and a high cell-turnover state can trigger drenching sweats. Cancer.gov

11. Fullness in the left upper belly. The spleen can enlarge from extra-medullary blood formation or leukemia infiltration. Rogel Cancer Center

12. Enlarged liver or lymph nodes (less common than in ALL). Spread beyond marrow can cause organ swelling. Cancer.gov

13. Gum swelling (gingival hypertrophy) or skin nodules (chloromas/myeloid sarcoma). Focal leukemic deposits can do this; more typical of monocytic subtypes but may occur. Cancer.gov

14. Headache, confusion, vision changes (rare). Very high white counts can cause sluggish blood flow (leukostasis) affecting brain/eyes. Cancer.gov

15. Bleeding complications during minor injuries or dental work. Platelet defects make hemostasis difficult. Cancer.gov

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Diagnostic tests

A) Physical-exam based

1. General look and vital signs. Doctors check pallor, fever, heart rate, breathing rate, and blood pressure. These show how sick the body is right now. Cancer.gov

2. Skin and mucosa check. They look for bruises, petechiae, and gum bleeding that point to low platelets. Rogel Cancer Center

3. Spleen and liver exam. Gentle pressing on the belly can detect enlargement from leukemia infiltration. Rogel Cancer Center

4. Lymph node exam. Swollen nodes suggest spread or infection that needs quick treatment. Cancer.gov

5. Bone tenderness. Pressing over bones may hurt if the marrow is crowded with blasts. Cancer.gov

B) “Manual” bedside maneuvers

6. Orthostatic blood pressure/heart-rate check. A big drop or fast rise when standing can reflect anemia or dehydration. (Helpful for safety planning.)

7. Capillary refill and nailbed check. Slow refill can support the picture of poor oxygen delivery from anemia.

8. Rumpel–Leede (tourniquet) test (rarely used). A blood pressure cuff is inflated briefly; many new petechiae may suggest fragile capillaries/low platelets.

9. Focused oral exam with tongue depressor. Simple inspection can show gum swelling, bleeding, or ulcers from neutropenia.

10. Bedside neurologic screen. Quick checks of strength, speech, and vision help detect leukostasis or CNS issues early.

C) Laboratory & pathology

11. Complete blood count (CBC) with differential. Shows anemia, thrombocytopenia, and circulating blasts. High or low white counts can both occur. Cancer.gov

12. Peripheral blood smear. A pathologist looks at cell shapes; Auer rods and blast features support AML; the amount of maturation looks “M1-like.” NCBI

13. Bone marrow aspirate and biopsy. The core test: confirms ≥20% blasts (modern threshold) and “little maturation” (M1-pattern) and allows all advanced studies. NCBI

14. Cytochemical stains (MPO, Sudan Black B). ≥3% MPO/SBB-positive blasts proves myeloid lineage; M1 has this positivity but still lacks maturation; when <3%, it fits M0. MedscapePMC

15. Flow cytometry (immunophenotyping). Confirms myeloid markers (e.g., CD13, CD33, CD117, MPO) and excludes mixed-phenotype leukemia; can hint at monocytic differentiation. PMC

16. Cytogenetics/karyotype and FISH. Detects chromosomal changes (e.g., complex karyotype, RUNX1-RUNX1T1, CBFB-MYH11, PML-RARA, etc.) that drive WHO/ICC class and ELN risk. Cancer.govCollege of American Pathologists

17. Molecular testing (PCR/NGS). Looks for mutations (e.g., NPM1, FLT3-ITD/TKD, ASXL1, RUNX1, TP53, IDH1/2). These set prognosis and guide targeted therapy. ASH PublicationsPMC

D) Electrodiagnostic

18. 12-lead electrocardiogram (ECG). Not diagnostic of AML itself, but essential to assess heart rhythm before anthracycline-based chemotherapy, and to detect leukostasis-related strain or electrolyte issues.

19. Electroencephalogram (EEG) (selected cases). Rarely used; if seizures or altered mental status occur, EEG helps evaluate CNS complications while infection/leukostasis are treated.
    (These tests support safe care planning rather than proving AML.)

E) Imaging

20. Chest X-ray. Screens for infection, bleeding, or fluid overload in a febrile, breathless patient. Cancer.gov

21. Ultrasound abdomen. Confirms liver/spleen size and checks for portal or splenic vein issues if symptoms suggest them.

22. CT/MRI (site-directed). Used when chloroma/myeloid sarcoma is suspected in bone, skin, orbit, or CNS, or to assess complications. Cancer.gov

Non-pharmacological treatments

(15 physiotherapy items, plus mind-body, “gene”/education-style self-management, and practical care. Each lists: description, purpose, mechanism, benefits.)

Note: These support medical therapy; they do not replace chemotherapy/targeted drugs.

1) Energy-conservation physiotherapy (fatigue plan)
Description (≈120–150 words): A rehab plan that maps your daily tasks and breaks them into smaller, paced steps. It trains you to alternate activity and rest, plan high-energy tasks for “good hours,” use stools for seated tasks, and simplify movements (e.g., rolling carts, shower chairs). You learn breathing, posture, and gentle pacing during chemotherapy days and neutropenic periods.
Purpose: Reduce exhaustion during treatment.
Mechanism: Balances oxygen use and muscle effort; avoids “boom-and-bust” cycles that worsen fatigue.
Benefits: Better daily function, less crash fatigue, safer movement.

2) Gentle aerobic walking (targeted for counts-aware days)
Description: 10–20 minutes of low-intensity walking on days your clinician approves, with masks in public and avoidance of crowded indoor spaces during neutropenia. Add intervals of slow–slower pace rather than fast bursts.
Purpose: Maintain heart-lung fitness and mood.
Mechanism: Improves mitochondrial efficiency and circulation without stressing low blood counts.
Benefits: Less deconditioning, better sleep and appetite.

3) Breathing physiotherapy (diaphragmatic + incentive breathing)
Description: Structured belly breathing, 4–6 cycles/min, and incentive-spirometer practice several times daily, especially during hospital stays.
Purpose: Prevent atelectasis and support oxygenation.
Mechanism: Recruits alveoli and improves ventilation.
Benefits: Fewer respiratory complications, calmer anxiety.

4) Range-of-motion & joint mobility
Description: Daily shoulder, hip, and ankle mobility (5–10 minutes) to counter bedrest stiffness.
Purpose: Preserve pain-free movement.
Mechanism: Lubricates joints, maintains muscle length.
Benefits: Easier transfers, less fall risk.

5) Light resistance band training
Description: Supervised 2–3 sessions/week using low-tension bands for large muscle groups when platelets and hemoglobin are safe.
Purpose: Maintain muscle mass.
Mechanism: Stimulus for protein synthesis without heavy loads.
Benefits: Stronger function, better glucose control.

6) Balance & fall-prevention drills
Description: Static and dynamic balance tasks, safe home setup (grab bars, clear floors, night lights).
Purpose: Avoid falls during anemia-related dizziness.
Mechanism: Trains proprioception and reaction.
Benefits: Fewer injuries and hospitalizations.

7) Neuropathy-friendly foot care & gait training
Description: Foot inspection routines, wide-toe shoes, gentle calf/foot stretches, and gait cues if chemo-related neuropathy develops.
Purpose: Prevent sores and tripping.
Mechanism: Protects sensory-impaired feet and improves step pattern.
Benefits: Safer walking, less pain.

8) Posture & core stabilization
Description: Short daily sessions (planks on knees, wall angels) tailored to fatigue.
Purpose: Reduce back/neck pain from bedrest.
Mechanism: Activates stabilizers and aligns spine.
Benefits: Comfort and better endurance.

9) Lymphedema/edema self-management
Description: Elevation, ankle pumps, soft compression (if approved), and salt moderation for fluid shifts.
Purpose: Limit swelling discomfort.
Mechanism: Aids venous/lymphatic return.
Benefits: Easier shoe fit, less heaviness.

10) Prehabilitation before intensive chemo/transplant
Description: 2–4 weeks of tailored cardio, strength, nutrition, and airway hygiene before induction or transplant, when timing allows.
Purpose: Enter treatment fitter.
Mechanism: Builds reserve to tolerate complications.
Benefits: Shorter stays, faster recovery.

11) Safe-movement education around central lines/ports
Description: Training to protect PICC/port during stretching and bathing; lifting limits; line-secure strategies.
Purpose: Prevent line dislodgement/infection.
Mechanism: Reduces traction and contamination.
Benefits: Fewer line issues, uninterrupted therapy.

12) Mucositis oral-care protocol
Description: Soft brush, bland rinses (saline/sodium bicarb), lip balm; avoid alcohol mouthwash; cryotherapy with ice chips during certain chemo if advised.
Purpose: Lower mouth sores and infection risk.
Mechanism: Protects mucosa and lowers microbial load.
Benefits: Less pain, better nutrition.

13) Sleep hygiene + fatigue timing
Description: Fixed bed/wake times, low-light evening routine, limit daytime naps to <30 min, manage steroids-related insomnia with schedule.
Purpose: Improve restorative sleep.
Mechanism: Resets circadian cues.
Benefits: Better energy and mood.

14) Infection-control coaching (home & hospital)
Description: Hand hygiene, food safety, mask use in crowds, pet and garden precautions, neutropenic diet advice during high-risk windows.
Purpose: Cut infection risk when ANC is low.
Mechanism: Reduces exposure to pathogens.
Benefits: Fewer febrile neutropenia episodes.

15) Bleeding-risk safety plan
Description: Platelet-aware brushing/flossing, electric shaver, fall-risk mitigation, medication review for NSAIDs/herbals.
Purpose: Prevent bleeding during thrombocytopenia.
Mechanism: Minimizes trauma and platelet inhibition.
Benefits: Less gum/nose bleed, fewer transfusions.

Mind-Body and Education-focused supports

16) Psycho-oncology counseling (CBT-based)
Description: Structured sessions to reframe fear, manage uncertainty, and set coping behaviors; includes crisis planning and caregiver support.
Purpose: Lower distress and depression.
Mechanism: Cognitive restructuring and behavioral activation.
Benefits: Better adherence, quality of life.

17) Mindfulness/meditation & guided imagery
Description: 10–15 minutes/day of breath-focused practice; guided imagery for procedures.
Purpose: Ease anxiety, pain, and insomnia.
Mechanism: Down-regulates sympathetic arousal.
Benefits: Calmer mood, lower perceived pain.

18) Acceptance & commitment strategies (ACT)
Description: Values-based goal setting despite uncertainty; brief exercises you can do in bed.
Purpose: Build resilience.
Mechanism: Psychological flexibility and defusion.
Benefits: Improved coping and participation.

19) Peer support & survivorship education
Description: Groups or 1-to-1 with AML peers; modules on labs, counts, what “ANC” and “MRD” mean.
Purpose: Normalize experience and build knowledge.
Mechanism: Social learning and self-efficacy.
Benefits: Confidence and informed decisions.

20) Treatment-literacy coaching (teach-back)
Description: Short teach-back sessions on consent forms, chemo days, drug names, and emergency signs.
Purpose: Ensure understanding.
Mechanism: Close knowledge gaps.
Benefits: Fewer errors and delays.

21) Nutrition counseling (counts-aware)
Description: High-protein, high-calorie options; safe-food handling; neutropenia-friendly produce washing.
Purpose: Maintain weight and healing.
Mechanism: Adequate macros/micros for marrow recovery.
Benefits: Sustained energy and fewer interruptions.

22) Financial and work-return navigation
Description: Help with disability forms, paid leave, and phased return to work/school.
Purpose: Reduce financial toxicity.
Mechanism: Early planning and resource linkage.
Benefits: Lower stress and better continuity.

23) Fertility counseling
Description: Early referral for sperm banking or oocyte/embryo preservation when feasible.
Purpose: Protect future family choices.
Mechanism: Time-sensitive gamete preservation.
Benefits: Peace of mind and options.

24) Infection-safe home exercise kits
Description: Cleanable bands, pedometer, step counters; avoid shared gym gear during neutropenia.
Purpose: Keep moving safely.
Mechanism: Controlled exposure and hygiene.
Benefits: Fitness without added risk.

25) Caregiver skills training
Description: Teaching caregivers symptom logs, safe meal prep, central-line checks, and when to call the team.
Purpose: Improve home safety.
Mechanism: Standardized checklists.
Benefits: Faster recognition of complications.

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Drug treatments

Dosing varies by age, kidney/liver function, comorbidities, and protocol. Always follow institutional protocol and drug labels.

1) Cytarabine (“Ara-C”)
Class: Antimetabolite. Dose/Time: Commonly 100–200 mg/m²/day by continuous IV infusion for 7 days in “7+3”; high-dose (HiDAC) 1.5–3 g/m² q12h on select consolidation cycles. Purpose: Core of induction and consolidation. Mechanism: Inhibits DNA polymerase; kills dividing myeloblasts. Side effects: Myelosuppression, mucositis, nausea, cerebellar toxicity (at high doses), conjunctivitis (needs steroid eye drops). ASH PublicationsNCCN

2) Daunorubicin
Class: Anthracycline. Dose/Time: 60–90 mg/m² IV days 1–3 with cytarabine. Purpose: Additive cytotoxicity in 7+3. Mechanism: DNA intercalation/topoisomerase II inhibition. Side effects: Myelosuppression, alopecia, mucositis, cardiomyopathy (cumulative dose). ASH Publications

3) Idarubicin
Class: Anthracycline. Dose/Time: 12 mg/m² IV days 1–3 as an alternative to daunorubicin in 7+3. Purpose: Induction. Mechanism: Similar to daunorubicin. Side effects: Myelosuppression, cardiotoxicity, mucositis. ASH Publications

4) CPX-351 (liposomal daunorubicin/cytarabine)
Class: Liposomal fixed-ratio chemotherapy. Dose/Time: 44/100 mg/m² IV on days 1, 3, 5 for induction; days 1, 3 for consolidation (esp. therapy-related AML/AML-MRC). Purpose: Improve delivery/synergy. Mechanism: Fixed 1:5 molar ratio in liposomes increases uptake in AML cells. Side effects: Prolonged cytopenias, infection risk. NCCN

5) Venetoclax (with HMAs or low-dose cytarabine)
Class: BCL-2 inhibitor. Dose/Time: Ramp-up to 400 mg PO daily; combined with azacitidine 75 mg/m² D1–7 or decitabine 20 mg/m² D1–5 in 28-day cycles for unfit/older adults; schedules often modified around counts. Purpose: Less-intensive yet deep remissions. Mechanism: Triggers apoptosis in blasts. Side effects: Cytopenias, tumor lysis, GI upset; drug–drug interactions. PMC

6) Azacitidine
Class: Hypomethylating agent (HMA). Dose/Time: 75 mg/m² SC/IV D1–7 q28d; often with venetoclax. Purpose: Induction/maintenance for less-fit patients. Mechanism: DNA hypomethylation reactivates silenced genes, promotes differentiation/apoptosis. Side effects: Cytopenias, injection-site reactions, nausea. NCCN

7) Decitabine (incl. 5-day or 10-day schedules)
Class: HMA. Dose/Time: 20 mg/m² IV D1–5 (or D1–10) q28d; commonly with venetoclax. Purpose: Less-intensive backbone. Mechanism: Similar to azacitidine. Side effects: Cytopenias, infections. NCCN

8) Midostaurin
Class: Multikinase/FLT3 inhibitor. Dose/Time: 50 mg PO BID on days 8–21 added to 7+3 and during consolidation; some centers use maintenance. Purpose: For FLT3-mutated AML (ITD/TKD) in fit patients. Mechanism: Inhibits FLT3 signaling. Side effects: Nausea, rash, cytopenias, QT effects (rare). NCCN

9) Quizartinib (Vanflyta)
Class: FLT3 inhibitor. Dose/Time: With standard induction (7+3) and consolidation, then maintenance monotherapy in newly diagnosed FLT3-ITD-positive adults per label. Dosing is protocol-specific and QT-monitored. Purpose: Improve survival in FLT3-ITD AML. Mechanism: Selective FLT3 inhibition. Side effects: QT prolongation, cytopenias. U.S. Food and Drug AdministrationCancer.gov

10) Gilteritinib
Class: FLT3 inhibitor. Dose/Time: 120 mg PO daily for relapsed/refractory FLT3-mutated AML. Purpose: Targeted salvage therapy. Mechanism: Inhibits FLT3 and AXL. Side effects: Transaminitis, diarrhea, differentiation syndrome (rare), QT prolongation. NCCN

11) Ivosidenib
Class: IDH1 inhibitor. Dose/Time: 500 mg PO daily ± azacitidine depending on setting. Purpose: IDH1-mutated AML (frontline unfit or R/R). Mechanism: Blocks mutant IDH1 to reduce 2-HG, allowing blast differentiation. Side effects: Differentiation syndrome, QT prolongation, leukocytosis. NCCN

12) Enasidenib
Class: IDH2 inhibitor. Dose/Time: 100 mg PO daily in IDH2-mutated AML. Purpose: Promote differentiation in R/R or selected frontline settings. Mechanism: Blocks mutant IDH2 → lowers 2-HG. Side effects: Differentiation syndrome, hyperbilirubinemia. NCCN

13) Gemtuzumab ozogamicin (GO)
Class: Anti-CD33 antibody-drug conjugate. Dose/Time: Often 3 mg/m² on days 1, 4, 7 with induction in CD33-positive, favorable-risk AML (e.g., core-binding factor); schedules vary. Purpose: Depth of remission. Mechanism: Delivers calicheamicin to CD33+ blasts. Side effects: Cytopenias, infusion reactions, veno-occlusive disease risk. NCCN

14) Glasdegib + low-dose cytarabine
Class: Hedgehog pathway inhibitor. Dose/Time: Glasdegib 100 mg PO daily + cytarabine 20 mg SC BID D1–10 q28d for unfit patients where VEN-HMA isn’t suitable. Purpose: Less-intensive regimen. Mechanism: Inhibits SMO to impair leukemic stem cell signaling. Side effects: Dysgeusia, muscle spasms, cytopenias. NCCN

15) Revumenib (Revuforj)
Class: Menin inhibitor. Dose/Time: FDA-approved (Nov 15, 2024) for relapsed/refractory acute leukemia with KMT2A (MLL) translocation; tablets (110 mg/160 mg) are available in the U.S.; exact dose per label and interaction profile must be followed. As of June 2025, FDA priority review is underway for NPM1-mutated R/R AML. Purpose: Target menin-KMT2A/NPM1 oncogenic program. Mechanism: Disrupts menin interactions to restore differentiation. Side effects: Differentiation syndrome, QT prolongation, cytopenias, LFT changes. U.S. Food and Drug AdministrationReutersAML Hub

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Dietary “molecular” supplements

Evidence in AML is supportive/adjunctive; avoid during neutropenia if infection risk from raw products; check for drug interactions (especially with venetoclax, azoles).

1) Vitamin D3
Dose: 1000–2000 IU/day (or per deficiency protocol). Function/mechanism: Immune modulation, bone/muscle support; low levels link to worse fatigue. Role: Correct deficiency; monitor calcium. Note: Avoid megadoses without labs.

2) Omega-3 (EPA/DHA)
Dose: 1–2 g/day combined EPA+DHA with food. Mechanism: Anti-inflammatory lipid mediators; may support cardiovascular health during therapy. Caution: Bleeding risk when platelets very low.

3) Whey or plant protein
Dose: 20–30 g per serving to hit 1.2–1.5 g/kg/day protein. Mechanism: Supplies amino acids for marrow recovery and muscle maintenance. Note: Choose pasteurized, safe products.

4) Zinc
Dose: 8–11 mg/day (avoid chronic high doses). Mechanism: Supports mucosal healing and immunity. Caution: Excess zinc can lower copper.

5) Probiotics (with caution)
Dose: As advised only when ANC is adequate and clinician approves. Mechanism: Gut barrier support; may reduce antibiotic-associated diarrhea. Caution: Rare bacteremia risk in profound neutropenia.

6) Glutamine (oral)
Dose: 10–30 g/day divided. Mechanism: Fuel for enterocytes; may ease mucositis in some settings. Caution: Discuss with oncology team.

7) Selenium (repletion if low)
Dose: Typically 55 mcg/day; avoid high doses. Mechanism: Antioxidant enzyme cofactor (GPx); supports redox balance. Caution: Narrow safety window.

8) Folate & B-complex (when deficient)
Dose: Folate 400–1000 mcg/day as needed. Mechanism: Supports DNA synthesis in recovering marrow (do not self-treat macrocytosis without labs).
9) Magnesium (replete if low)
Dose: 200–400 mg/day as tolerated. Mechanism: Neuromuscular stability, cardiac rhythm support (some agents affect QT).
10) Oral rehydration (electrolyte solutions)
Dose: Sips through the day during diarrhea/fever. Mechanism: Maintains volume and electrolytes.

(Because supplement evidence evolves and interactions are real, align with your oncology pharmacist/dietitian.)

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Immunity/regenerative/stem-cell–related” medicines

1) Filgrastim (G-CSF) — Dose: ~5 mcg/kg/day SC until ANC recovery. Function: Stimulates neutrophil production after chemo. Mechanism: Binds G-CSF receptor on precursors.
2) Pegfilgrastim — Dose: Single SC dose post-chemo per cycle. Function: Longer-acting G-CSF.
3) Sargramostim (GM-CSF) — Dose: Per protocol. Function: Broader myeloid stimulation; sometimes in post-transplant settings.
4) Epoetin alfa/Darbepoetin — Function: Red cell support in selected anemias; not during induction unless protocol-driven.
5) IVIG — Function: Passive immunity in hypogammaglobulinemia with recurrent infections.
6) Allogeneic hematopoietic stem cell transplant (HSCT) “drug-free” concept — Not a drug, but the central regenerative therapy: donor stem cells re-establish normal hematopoiesis; conditioning regimens eradicate leukemia and allow engraftment; GVHD prophylaxis modulates immunity. (Details below under surgeries/procedures.) NCCN

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Surgeries / procedures

1) Allogeneic HSCT
Procedure: Conditioning chemo ± radiation, donor stem-cell infusion via central line, inpatient monitoring for engraftment and GVHD prevention.
Why: Offers the best chance of cure for many intermediate/high-risk AML patients in first remission or later, guided by genetics and MRD. NCCNASH Publications

2) Central venous catheter/port placement
Procedure: Minor surgery to place a tunneled line or port for chemo, transfusions, labs.
Why: Reliable access and fewer needle sticks.

3) Leukapheresis (for hyperleukocytosis)
Procedure: Apheresis machine removes circulating blasts rapidly.
Why: Short-term cytoreduction to reduce leukostasis risk while chemo starts.

4) Splenectomy (rare)
Procedure: Surgical removal of the spleen.
Why: Considered only in unusual cases with massive hypersplenism causing transfusion-refractory cytopenias or pain.

5) Fertility preservation procedures
Procedure: Sperm banking or oocyte retrieval/embryo cryopreservation before therapy when time allows.
Why: Protects future fertility.

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Prevention strategies

1. Prompt care for fevers ≥38.0 °C during neutropenia.

2. Hand hygiene and masks in crowds; avoid sick contacts.

3. Food safety: well-cooked meats/eggs; careful produce washing; avoid unpasteurized items during neutropenia.

4. Vaccination plan: inactivated vaccines as advised; live vaccines only when immune system has recovered and team approves (post-transplant schedules are specialized).

5. Oral care: soft brush, bland rinses; dental consult pre-chemo if possible.

6. Bleeding precautions when platelets low (no NSAIDs, use electric shaver).

7. Skin care: moisturize; treat cuts promptly; avoid gardening/soil during severe neutropenia.

8. Safe exercise with fall prevention; avoid heavy lifting when counts/line status make it unsafe.

9. Medication review: check herbals/supplements for interactions (e.g., with venetoclax/azoles).

10. Adherence and lab follow-up: keep chemo schedules, transfusion visits, and MRD checks. NCCN

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When to see doctors

• Fever ≥38.0 °C, chills, or any signs of infection (sore throat, cough, burning urination).

• Bleeding (nosebleed that won’t stop, black stools, blood in urine), new bruising or petechiae.

• Shortness of breath, chest pain, severe headache, confusion, sudden weakness.

• Severe mouth sores, inability to drink or keep fluids down; diarrhea >4 stools/day.

• Line problems: redness, swelling, discharge, or pain at catheter/port site.

• New rash, swelling of face/tongue, or allergic/drug reaction symptoms.

• After transplant: any signs of GVHD (new rash, jaundice, severe diarrhea).

• Any sudden change that feels serious or “not right.” (Better to call early.)

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What to eat and what to avoid

What to eat

1. Protein-rich foods (eggs, dairy, tofu, fish well cooked) to hit daily protein goals.

2. Soft, high-calorie options during mucositis (yogurt, smoothies with pasteurized ingredients, blended soups).

3. Cooked vegetables/grains; peeled fruits thoroughly washed.

4. Electrolyte fluids during diarrhea/fever.

5. Small, frequent meals to fight nausea and early fullness.

What to avoid

1. Raw/undercooked meat, eggs, fish; unpasteurized dairy/juices during neutropenia.
2.  Salad bars/buffets and deli meats unless reheated steaming hot.
3.  Alcohol (especially when platelets low or on hepatotoxic drugs).
4. Grapefruit/Seville orange products with certain targeted drugs (CYP3A interactions).
5. Herbal products that raise bleeding risk or interact with chemo (e.g., high-dose turmeric, St John’s wort—always check). NCCN

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Frequently asked questions

1) Is FAB M1 different from other AML types?
Yes—FAB M1 is defined by minimal maturation of myeloid blasts. Today, genetic mutations matter more for choosing drugs and estimating risk than FAB alone. MedscapeASH Publications

2) What is induction therapy?
The first phase to clear blasts from marrow—often 7+3 for fit patients, or HMA+venetoclax for less-fit patients. NCCN

3) How do doctors decide on transplant?
They combine genetics, remission status, MRD, age, and fitness. Higher-risk genetics often favor allogeneic HSCT in first remission. ASH Publications

4) What targeted drugs might I receive?
Examples: FLT3 inhibitors (midostaurin, quizartinib, gilteritinib), IDH1/2 inhibitors (ivosidenib, enasidenib), menin inhibitor (revumenib) for KMT2A-rearranged leukemia; choices depend on your mutations and disease phase. U.S. Food and Drug Administration+1Cancer.gov

5) Is revumenib approved yet?
Yes—for R/R acute leukemia with KMT2A translocation (Nov 15, 2024). In June 2025, the FDA accepted priority review for R/R NPM1-mutant AML (decision pending). U.S. Food and Drug AdministrationAML Hub

6) Will I lose my hair?
Often, yes, with anthracyclines. Hair usually regrows after therapy ends.

7) How are infections prevented?
Growth factors, careful hygiene, sometimes antibacterial/antifungal/antiviral drugs, and fast evaluation of fever. NCCN

8) What is “differentiation syndrome”?
A potentially serious reaction when blasts mature quickly (seen with IDH and menin inhibitors). Symptoms include fever, fluid in lungs, and low blood pressure; urgent steroids treat it. NCCN

9) How is response measured?
Blood counts, bone marrow exams, and MRD testing by flow/PCR/NGS after induction and later cycles. NCCN

10) What if I am not fit for intensive chemo?
You may receive venetoclax + azacitidine/decitabine or glasdegib + low-dose cytarabine, with strong supportive care. PMC

11) Can I work during treatment?
Many people cannot during induction. Some return part-time during consolidation or maintenance; plan with your team.

12) Are clinical trials important?
Yes—trials offer access to new targeted or immunotherapies and are central to AML progress. Ask at each phase.

13) What is maintenance therapy?
Low-intensity treatment (e.g., oral azacitidine in some settings, or quizartinib maintenance in FLT3-ITD regimens per label) to reduce relapse after remission. U.S. Food and Drug Administration

14) How long does treatment last?
Induction (weeks), then consolidation or transplant (months). Monitoring continues for years.

15) What is my outlook?
Prognosis depends on age/fitness, genetics (FLT3, NPM1, etc.), MRD, and transplant access. Your team uses ELN risk to discuss personalized outcomes. ASH Publications

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 07, 2025.

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